Previous research had suggested that dysfunction of neuronal mitochondria -- the energy-producing subcellular organelles -- occurs in the brains of MS patients with progressive clinical disability. However, the molecular mechanisms underlying this process remained elusive.
"Because the brain is bathed by the cerebrospinal fluid (CSF), we asked whether treating cultured neurons with the CSF from MS patients with a relapsing/remitting or a progressive disease course would possibly elicit different effects on neuronal mitochondrial function," said the study's primary investigator Patrizia Casaccia, Einstein Professor of Biology at The Graduate Center and founding director of the Neuroscience Initiative at the ASRC. "We detected dramatic differences in the shape of the neuronal mitochondria and their ability to produce energy. Only exposure to the CSF from progressive MS patients caused neuronal mitochondria to fuse and elongate while rendering them unable to produce energy. We therefore searched for potential mechanisms of CSF-induced neurodegeneration with the intent to define therapeutic strategies."
CSF - Samples - Patients - MS - MS
CSF samples were acquired from 15 patients with relapsing/remitting MS and 29 with progressive MS. These samples were extensively characterized, both functionally and metabolically. Video recordings of live, cultured rat neurons that were exposed to the CSF revealed important differences. Researchers detected a characteristic elongation of mitochondria exposed to CSF samples from progressive MS patients. This characteristic response was not present in mitochondria exposed to CSF from patients with a relapsing/remitting MS. Biochemical characterization of mitochondrial activity further...
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